Abstract
The study investigated the protective effect of walnut oligopeptides (WOPs) against ethanol-induced gastric injury using Sprague-Dawley (SD) rats. Rats were randomly divided into seven groups based on body weight (10/group), normal group, ethanol group, whey protein group (220 mg/kg body weight), omeprazole group (20 mg/kg body weight), and three WOPs groups (220, 440, 880 mg/kg body weight). After 30 days of treatment with WOPs, rats were given 5 mL/kg absolute ethanol by gavage to induce gastric mucosal injury. Gastric ulcer index (GUI) were determined and the following measured; gastric content pH, gastric mucin, endogenous pepsinogens (PG), prostaglandin E2 (PGE2), inflammatory cytokines, oxidative stress indicators, and the expression of apoptosis-related proteins were measured to evaluate the gastroprotective effect of WOPs. The results showed that the administration with WOPs markedly mitigated the hemorrhagic gastric lesions caused by ethanol in rats, and decreased the GUI, the gastric content pH, PG1, PG2, and NO levels, enhanced mucin and PGE2. Also, WOPs repressed gastric inflammation through the reduction of TNF-α, IL-6, IL-1β and increase IL-10 levels, and revealed antioxidant properties with the enhancement of superoxide dismutase, glutathione, and catalase activity, while reduction of malondialdehyde. Moreover, WOPs treatment significantly down-regulated Bax, caspase-3 and nuclear factor-κB p65 (NF-κB p65) expression, while up-regulating the expression of Bcl-2 and inhibitor kappa Bα (IκBα) protein. These results indicated that WOPs have protective effects against ethanol-induced gastric mucosal injury in rats through anti-inflammatory, anti-oxidation, and anti-apoptosis mechanisms.
Highlights
Gastric ulcers, characterized by mucosal damage, are induced by nonsteroidal anti-inflammatory drugs, potassium chloride, alcohol intake, and Helicobacter pylori, etc., [1]
During the 30 days of the experiment, it was observed that daily intervention of walnut oligopeptides (WOPs) did not cause any signs of toxicity or mortality in rats, and there was no significant difference in the bodyweight among all groups (p > 0.05)
The total food intake was significantly higher in WOPs-HG groups than that in the normal control, ethanol, and whey protein group (p < 0.05), but no significant change in food utilization was observed between groups (p > 0.05) (Table 2)
Summary
Gastric ulcers, characterized by mucosal damage, are induced by nonsteroidal anti-inflammatory drugs, potassium chloride, alcohol intake, and Helicobacter pylori, etc., [1]. Ethanol is one of the most common gastric mucosal invasion factors. With the development of society and increased consumption of alcohol, the ethanol-induced gastric ulcer has become a prominent gastrointestinal disease [2]. World Health Organization report showed that drinking alcohol caused about 3 million deaths globally in 2016 (about 2.3 million men and about 700,000 women), accounting for 5.3 percent of all deaths. Diseases of the digestive system accounted for 21.3 percent of deaths attributable to alcohol consumption, placing a huge burden on global public health [3].
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